Tuesday, October 25, 2011

Doug, sorry I had so few answers for you in the ED. Had to go hit the books after we had that patient!

This isn't a comprehensive article on IIH, nor is it an efficient outline of the critical information for the boards, life, or pimping. It's just a list of 5 things that took me somewhat by surprise, that I had never learned, or that I swear I had learned as the opposite.

1. "Transient visual obscurations" - The predominant visual disturbance isn't a nice, clean visual field cut. Instead, over 70% of patients have really brief episodes (< 1 minute) of loss of acuity, provoked by standing, sitting, light, Valsalva, or extra-ocular movements. Yeah, you'll get field loss on perimetry, but the TVOs are what patients will actually complain of.

2. Sparkles - They can also get flashes, or photopsias, as well as the TVOs.They are described as "white or less commonly coloured small flashes, flickering lights, stars twinkling, or flashes in the periphery of the visual field

Simulation available

3. Patients with IIH also report an odd kind of noise inside their heads. It's termed "pulsatile tinnitus," but it only infrequently seems to be a high-pitched tone. More often, it's described as '"a rushing river', a waterfall or a buzzing, whistling or blowing sound."

4. You get imaging to r/o something else, like a not-so-pseudo tumor or a sinus venous thrombosis. It's not used to diagnose IIH. However, one finding that would be consistent with IIH would be small ventricles or an empty sella, according to some.

Flattened ventricles.

5. Perhaps the imaging study that we should be using more often is our ultrasound. Up until this month, the world's literature for using ultrasound to detect papilledema was limited to this study by Michael Stone (Download). While the case provided an example of using an optic nerve sheath diameter of >5 mm to make a diagnosis of increased ICP, it also demonstrated sonographic papilledema.

But now there are 2 new publications that provide more evidence that we should be dropping our old clinical skills (polished as they may be...) in favor of using newer technology!

1880 Loring opthalmoscope. Not new.

The first article is an abstract that was just published in the October issue of Annals of Emergency Medicine, the ACEP Research Forum 2011 supplement, and is entitled "Point-of-Care Ocular Sonography to Detect Optic Disc Swelling." (Download pdf)

The authors compared EP-performed ultrasound exams of the optic disc with those of an neuro-ophthalmologist, as well as optical coherence tomography.

Optic disc swelling as seen on OCT

For the study, 2 EPs hung out in a neuro-optho clinic, and did ocular US on a number of patients. They later compared their results with the specialist, who also had access to the OCT images and results. After 20 patients, they found they had "excellent correlation" between the OCT and height of the disc seen on ultrasound.

Another example of an elevated optic disc (small arrow)

Another article,still in-press at the American Journal of Emergency Medicine (by Daulaire et al.) (Download pdf), reviews a series of 3 headache patients who had apparent optic disc elevation on bedside US. The US results were considered confirmed, in each respective case, through a finding of elevated CSF pressure, an exam of the fundus by the ophthalmology service, and an MRI. There's a review of the technique, as well as of the scant literature.

So, the next time you have that odd headache patient, ask them about TVOs and photopsias, and put a probe on their eyes!

Saturday, October 22, 2011

It has come to my attention that the tenuous grasp I thought that I had possessed about cervicitis and PID became archaic at some point. My beloved, and much highlighted, text that was new when I started med school is now behind the times.

It is so 2004...

To be fair, the 2000's have been active in this area, and I think that you should hear a little bit about what's been goin' on.

First up: What are cervicitis and PID, i.e. what are the diagnostic criteria? This is important, because it turns out that in the ED we aren't so hot with the diagnosis of such things. Two studies point this out.

That's pus.

This study done in the Yale ED was written by your current boss (and with a future boss?), so you should probably know this!

Hint!

The paper, "Compliance with the CDC Recommendations for the Diagnosis and Treatment of Sexually Transmitted Diseases" (Download here), published in 2004, documented how essential elements in the history and physical exam where missing from the charts of patients who had been diagnosed with cervicitis or PID. Furthermore, incomplete or erroneous treatment was often provided. All in an ED we all know and love...

First off, about 25% of the patients diagnosed with cervicitis did not have documented physical findings that supported the diagnosis; i.e. they had neither a mucopurulent cervical discharge, nor a friable, easily bleeding cervix. Despite this over-diagnosis, they also found that 40% of the women who had been diagnosed with cervicitis actually had sufficient exam finding to meet PID criteria. So, they were also under-treating! Urgh.

Even better, they break the results down according to the site of treatment: the adolescent clinic or the children's ED, and no one comes off looking good. The ED misdiagnosed about half the time, and the clinic about a third.

So, let's get the definitions laid out, so there is no confusion. This all comes from the current CDC guide for STDs, which you can access online, or you can download the pdf.

Cervicitis:

"Two major diagnostic signs characterize cervicitis: 1) a purulent or mucopurulent endocervical exudate visible in the endocervical canal or on an endocervical swab specimen (commonly referred to as mucopurulent cervicitis or cervicitis) and 2) sustained endocervical bleeding easily induced by gentle passage of a cotton swab through the cervical os."

PID:

"Empiric treatment for PID should be initiated in sexually active young women and other women at risk for STDs if they are experiencing pelvic or lower abdominal pain, if no cause for the illness other than PID can be identified, and if one or more of the following minimum criteria are present on pelvic examination:

cervical motion tendernessor

uterine tendernessor

adnexal tenderness."

They note that in cases where a diagnosis based on these minimal criteria "might cause unnecessary morbidity," that a few other elements may be used to boost the specificity, namely a mucopurulent discharge or a fever.

Telling this guy that his 14 y.o. daughter has PID = morbidity?

By contrast, the 1998 CDC guidelines required that all 3 of the minimal criteria (CMT, uterine, and adnexal tenderness) be found in order to make a diagnosis. Why did this change? After all, it's not so often that we change a diagnosis. Femur fractures, for example, have never had a revision of the diagnostic criteria!

This was a major randomized trial, and I simply will not do justice summarizing it here. Instead of reading any more mind-numbing studies about subarachnoids or PEs, read this.

The trail was designed to examine the effectiveness of IV versus outpatient treatment of PID, but since they were collecting all this data on women with suspected PID, and then getting all these confirmatory tests, they wanted to see how sensitive and specific the elements of the CDC diagnostic criteria were. It was a multicenter trial, in both clinics and EDs throughout the US. Diagnostic techniques were comprehensive: PID was diagnosed histologically, from samples obtained from transcervical aspiration of endometrial tissue. In the end, they had complete information on 651 women, and the results were...

They found that the minimal CDC criteria (all 3 of CMT, adnexal, and uterine tenderness) was only 83% sensitive, with a specificity that wasn't exactly a selling point. Furthermore, if you were hoping that supporting elements, such as a fever (or it's absence) might help diagnosis, there were disappointing results.

For my part, the negative likelihood ratios for fever and purulent discharge grab my attention. The absence of the elements does not meaningfully help the diagnosis, since the negative LR is close to 1. Heck, even a negative NAAT test only cuts the probability in half!

In the discussion section, the authors offered their suggestion that "clinicians should consider empiric treatment of pelvic inflammatory disease in at-risk women with adnexal tenderness at presentation and no other obvious diagnosis," which is close to the current guidelines. And even with this incredibly liberal definition of PID, we are still going to miss about 5%!

So that's it for diagnosis. As for treatment, like all of ID, things change every year - look up the current reccs in the CDC guide I linked above. Some things are suprising (no more 125 of Rocephin!), and others stay the same (7 days of doxy for cervicitis, 14 for PID).This post is long enough, so I'll leave you with just one more cervix:

Thursday, October 6, 2011

I wanted to quickly review 2 issues that come up with regularity when a resident & I have a patient with ACS, either a STEMI or NSTEMI. Let me start with the conclusion first, and go from there.

1. Tachycardia is a reason not to give IV beta-blockers in the ED for NSTEMI or STEMI.

2. Heparin hasn't actually been shown to have much effect in NSTEMI.

Okay, first about the beta-blockers. There used to be a lot more enthusiasm for using IV metoprolol in the ED with a STEMI, and many clinicians still feel that they are obligated to give them. But a lot of that changed, first when the COMMIT trial came out, and then when the AHA modified their guidelines to reflect the new evidence. In that big trial, patients with a STEMI were given the IV metoprolol load in the ED, followed by PO. The kicker is that there was overall no difference in 28 day mortality, since for every person who apparently didn't have a reinfarct or fatal arrhythmia. there was an extra person who died of HF!

Make special note of the risk factors listed after the asterix, in small print, at the bottom: sinus tachycardia exceeding 110 bpm.

These considerations were extended to the NSTEMI guidelines as well, although the evidence base is not as direct or contemporary as it is for STEMI. The 2007 AHA UA/NSTEMI guidelines basically mirror those for STEMI with regard to PO beta-blockers (Class 1 in the first 24 hours) and IV beta-blockers (class 2a, with same contraindications as above).

As for heparin for NSTEMI, it is sort of absurd looking at the recommendations and the supporting evidence. The 2007 AHA UA/NSTEMI guidelines cite 2 studies in support of the use of UFH. The more recent, and larger, was this paper , a meta-analysis of 6 studies that looked at the benefit of adding heparin to aspirin in UA/NSTEMI.

Ok, look at the title. Seems like a pretty clear title - you know just what they found in their study, and you should expect to find at least statistical significance in the results, right?

Not really

Right there, first page - the RR for MI or death was not significantly reduced when heparin was added to aspirin. They include this helpful graph, which shows the results of 6 trials, and the summary estimate that they calculate.

In the last few sentences, the authors, note that "this meta-analysis of 6 randomized controlled trials demonstrated a strong trend toward reduction in risk of MI or death during randomized therapy in patients with unstable angina treated with aspirin plus heparin compared with those treated with aspirin alone." The phrase "strong trend" is not found in the conclusion of the abstract, but instead they highlight the "33% reduction" in outcomes.

Heparin probably has utility in the sicker subset of NSTEMI, the patients with positive enzymes, dynamic ECG changes, ongoing pain. But those are the kind of patients you're talking about with the cardiologist, calling CCU, and perhaps arranging same-day cath lab evaluation. But for the run o' the mill ACS patient, check out the evidence first.